Psychosocial stress inhibits additional stress-induced hyperexpression of NO synthases and IL-1β in brain structures

Background: The aim of this study was to compare the expression of interleukin-1 beta (IL-1 beta), neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) in the prefrontal cortex (PFC), hippocampus (HIP) and hypothalamus (HT) during chronic crowding (CS) (psychosocial) and restraint (RS) (physico-psychological) stress. Adaptational changes of these stress mediators to a subsequent acute RS, in two models of chronic stress were investigated. Methods: Rats were crowded (24 in one cage) or restrained in metal tubes for 10 min twice a day for 3, 7, and 14 consecutive days and decapitated. For determination of adaptational changes the chronically crowded and restrained rats 24 h after the last stress session were subjected to a single 10 min RS. The IL-1 beta, nNOS and iNOS protein levels in brain structures samples were analyzed by Western blot procedure. Results: Chronic CS for 3 days did not markedly change the subsequent acute stress induced expression of nNOS, iNOS and IL-1 beta protein level in PFC and iNOS protein level in HT. CS markedly decreased the expression of nNOS, iNOS and IL-1 beta in HIP. By contrast, parallel chronic RS, significantly increased the subsequent acute stress-induced expression of iNOS and IL-1 beta in PFC and considerably increased iNOS level in HT. Conclusion: Chronic psychosocial stress, may protect against possible harmful action of hyperproduction of iNOS and iNOS derived nitric oxide (NO) mainly in PFC and HIP. By contrast, chronic physico-psychosocial stress may strongly potentiate additional stress-induced harmful effects of NOS and IL-1 beta hyperproduction. (C) 2016 Published by Elsevier Sp. z o.o. on behalf of Institute of Pharmacology, Polish Academy of Sciences.